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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.01 seconds)

The endocrinological and biochemical mechanisms controlling energy expenditure in brown adipose tissue at the cellular as well as at the total tissue levels are briefly reviewed. Thermogenesis in brown adipose tissue is principally controlled by the activity of hormone-sensitive lipases that represent the 'flux-generating' step in the stimulus-calorigenesis sequence. Long chain fatty acids are the physiological messengers regulating mitochondrial respiration. Agents stimulating brown adipocyte lipolysis (catecholamines, glucagon, methylxanthines) also stimulate respiration, and conversely, agents inhibiting lipolysis (adrenergic antagonists, insulin, prostaglandins) also inhibit respiration. This indicates that lipolysis and respiration are functionally coupled in brown adipose tissue. On the other hand, brown adipose tissue thermogenic capacity increases during cold acclimation or adaptation to hyperphagia. Brown adipocyte proliferation and differentiation from precursor cells (interstitial cells and brown preadipocytes) represent the fundamental phenomena explaining the increase capacity of cold acclimated and/or hyperphagic animals for responding calorigenically to catecholamines. Physiological situations associated with a stimulation of energy expenditure and a negative energy balance (cold acclimation, exercise training, caffeine consumption) generally induce a stimulation of adipocyte proliferation in brown adipose tissue that is accompanied by a simultaneous inhibition of cell proliferation in white adipose tissue. The physiological significance of these metabolic adaptations is to modulate the capacity of homeothermic animals for energy expenditure in accordance with energy requirements.
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PMID:Regulation of energy expenditure in brown adipose tissue. 299 14

Long-term cafeteria feeding, cold exposure, and the combination of treatments increased energy intake in female Wistar rats by 25%, 113%, and 150%, respectively, in comparison with controls (P less than 0.01). Although cafeteria feeding at room temperature markedly increased the insulin response to an intravenous glucose tolerance test (IVGTT), glucose tolerance was deteriorated (P less than 0.01). In contrast, cold exposure significantly improved glucose tolerance in the presence of a reduced insulin response in Purina- and cafeteria-fed animals. Moreover, cold exposure also decreased body weight gain and increased brown adipose tissue mass, total cytochrome-oxidase activity, and cellularity by approximately 600-800%. The results suggest that cold exposure enhances insulin sensitivity of peripheral tissues, whereas hyperphagia on a high-fat, low-protein diet leads to insulin resistance. In addition, the results demonstrate that prolonged stimulation of energy expenditure by cold exposure not only reverses the diabetogenic effects of cafeteria feeding but also improves glucose tolerance. This phenomenon could result from a combination of two factors: (1) a cold-induced prevention of obesity; and (2) an enhanced disposal of circulating glucose into peripheral tissues, including brown adipose tissue.
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PMID:Cold exposure reverses the diabetogenic effects of high-fat feeding. 300 94

Rats fed a cafeteria diet to produce hyperphagia showed increases in the maximal thermogenic responses (rise in oxygen consumption) to isoprenaline (mixed beta-agonist), prenalterol (beta 1-selective agonist) and clenbuterol (beta 2-agonist), and left-shifts in the dose-response curves to the latter two. The maximal response to phenylephrine (alpha-agonist) was similar for control and cafeteria rats. Ligand binding studies revealed increases in beta-adrenoceptor density of 33-38% in brown fat cells and isolated membranes from cafeteria-fed rats, but a 30% reduction in beta-receptors in heart membranes. Cold-adaptation caused a 22% reduction in beta-receptor density in brown fat membranes, but no change in heart. The ratio of beta 1/beta 2-receptors in brown fat was reduced from 59/45 in control to 47/54 in cafeteria-fed rats, but was not significantly altered in heart (58/44) or in brown fat from cold-adapted animals (64/30). alpha-Adrenoceptor density was increased above control values by 69 and 25% in brown adipose tissue from cafeteria and cold-adapted rats, respectively.
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PMID:Thermogenic responses to adrenoceptor agonists and brown fat adrenoceptors in overfed rats. 301 44

Lateral hypothalamic damage impaired both physiological and behavioral responses of rats during exposure to a 5 degree C environment. The brain-damaged animals usually did not conserve heat in the cold as well as control rats did, nor did they always increase their caloric intake to meet their energy needs. However, when given sucrose solution to drink instead of water, they did increase their ingestion of chow in response to cold exposure. It is likely that the elevated consumption of palatable fluid served to relieve dehydration and thereby removed its constraints on eating, thus permitting hyperphagia to occur. In contrast to these results, rats with large dopamine-depleting brain lesions, produced by intraventricular 6-hydroxydopamine treatments, always increased food intake when exposed to cold stress and demonstrated no apparent problems in peripheral vasoconstriction. Thus, it is unlikely that striatal dopamine depletions account for either the impaired feeding response or the inadequate heat conservation of rats with lateral hypothalamic lesions during cold stress.
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PMID:Effects of lateral hypothalamic lesions on food intake of rats during exposure to cold. 304 32

Body energy balance is regulated in adults. The accuracy of the phenomenon is particularly evident in laboratory animals under steady conditions. Moreover, it has been repeatedly demonstrated that this balance is maintained in spite of fluctuations in food intake or energy expenditure. When animals such as rats, dogs or rabbits are presented with a diluted or concentrated version of familiar food, they compensate rapidly by increasing or decreasing their ponderal intake. This is achieved first by a change in meal frequency, then meal size adapts to the new caloric content and meal frequency returns to the original pattern. This adaptation is based on the learning of post-ingestive cues. Hypo or hyperphagia leads to reduced or increased energy expenditure, as the case may be; the basal metabolic rate is modulated by thyroid hormones and diet-induced thermogenesis by the sympathetic system. These variations are partly regulatory. In a cold environment, the increase in energy expenditure caused by increased thermogenesis is rapidly compensated by increased caloric intake. Physical activity activates the sympathetic system responsible for numerous hormonal changes, the most important of which is insulin hyposecretion. In animals or humans, moderate aerobic exercise induces a small weight loss; afterwards, weight gain is normalized and increased caloric intake compensates for energy expenditures such as exercise, increased basal metabolic rate and diet-induced thermogenesis. Extreme changes in body weight and fat are produced by gestation and lactation; they are satisfactorily explained by concomitant hormonal changes. Especially during lactation, food intake is regulated so that it allows body weight to return to pregestation level. Studies on the mechanisms implicated in the regulation of body energy balance are still in progress. Friedman and Ramirez (1985) suggest that the way fatty acids are utilized is important. Kasser et al. (1985) show a striking difference in the cellular metabolism of hypothalamic regions, depending on the metabolic state or the animal, and Woods et al. (1985) strongly suggest a role for the central insulin level. These hypotheses are well-documented and not exclusive of each other.
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PMID:[Adaptation of food ingestion to energy expenditure]. 355 Sep 78

Sympathetic activity has been assessed, by measurements of norepinephrine turnover, in interscapular brown adipose tissue of mice during lactation. Norepinephrine turnover was reduced in brown adipose tissue from early lactation until weaning. The reduction in turnover occurred in dams suckling either large-or small-sized litters. Norepinephrine turnover returned to the control level after natural weaning and increased rapidly after abrupt weaning at peak lactation. Acute exposure to cold resulted in a large increase in norepinephrine turnover in brown adipose tissue of lactating mice, as in control animals. These results indicate that sympathetic activity is suppressed in brown adipose tissue during lactation, but sympathetic responsiveness is retained. The reduction in sympathetic activity is likely to be responsible for the decrease in brown adipose tissue thermogenesis in lactation. Norepinephrine turnover in the heart tended to be reduced at peak lactation, suggesting that there may be a general decrease in sympathetic activity in the lactating animal. In contrast to the normal animal, the hyperphagia of lactation does not lead to an activation of the sympathetic nervous system.
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PMID:Sympathetic activity in brown adipose tissue in lactating mice. 368 22

The mechanisms of brown adipocyte proliferation and differentiation during cold acclimation (and/or adaptation to hyperphagia) have been studied by quantitative photonic radioautography. [3H]thymidine was injected to warm-acclimated (25 degrees C) rats and to animals exposed to 5 degrees C for 2 days. Samples of interscapular brown adipose tissue were collected for quantitative analysis of mitotic frequencies at various periods of time (4 h-15 days) after the injection of [3H]thymidine, the rats being maintained at the temperatures to which they were initially exposed. Confirming our previous results [Bukowiecki et al., Am. J. Physiol. 242 (Endocrinol. Metab. 5): E353-E359, 1982], it was found that cold exposure for 2 days markedly enhanced mitotic activity in endothelial cells, interstitial cells, and brown preadipocytes rather than in fully differentiated brown adipocytes. The total tissue labeling index (percent of labeled nuclei) increased approximately 70 times over control values. We now report that cellular labeling progressively increased in mature brown adipocytes during cold acclimation, whereas it correspondingly decreased in interstitial cells and brown preadipocytes. This indicates that the sequence of events for cellular differentiation is interstitial cells----brown preadipocytes----mature brown adipocytes. Remarkable, labeling frequency did not change in endothelial cells during cold acclimation demonstrating that these cells cannot be considered as progenitors of brown adipocytes. It is suggested that brown adipocyte proliferation and differentiation from interstitial cells represent the fundamental phenomena explaining the enhanced capacity of cold-acclimated and/or hyperphagic rats to respond calorigenically to catecholamines.
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PMID:Proliferation and differentiation of brown adipocytes from interstitial cells during cold acclimation. 371 29

The present study assessed in rats the effects of muscarinic receptor antagonism upon analgesia induced by cold-water swims (CWS: 2 degrees C for 3.5 min) and 2-deoxy-D-glucose (2DG: 600 mg/kg). First, CWS analgesia was significantly reduced 30 min after the swim by scopolamine (0.01 and 0.1 mg/kg) and methylscopolamine (10 mg/kg) pretreatment, and was eliminated 60 min after the swim by scopolamine (0.01-10 mg/kg) and methylscopolamine (1,10 mg/kg) pretreatment. In contrast, scopolamine potentiated CWS hypothermia. Second, while scopolamine (1 mg/kg) and methylscopolamine (1,10 mg/kg) pretreatment prolonged 2DG analgesia, both antagonists dose-dependently reduced 2DG hyperphagia. Third, the changes in analgesic and hypothermic stress responses were not due to baseline shifts in jump thresholds or body temperatures. However the dose-dependent reductions by scopolamine and methylscopolamine in baseline food intake and 2DG hyperphagia were significantly correlated. Fourth, the dose-dependent reduction by scopolamine and methylscopolamine of pilocarpine analgesia differed in pattern from the other analgesic effects, suggesting heterogeneity in muscarinic receptor modulation of different analgesic responses.
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PMID:Effects of muscarinic receptor antagonism upon two forms of stress-induced analgesia. 374 24

A new strain of genetically obese mouse, the dbPas mouse, has been studied in terms of fat pad cellularity, serum parameters and thermogenesis. This obesity was observed in the inbred DW strain of mice at the Institut Pasteur-France, and is due to a recessive mutation on chromosome 4 at the diabetes locus. The mice became grossly obese, gaining weight until at least 16 mo of age. By 6 mo of age they exhibited hyperphagia, hypercholesterolemia, severe hyperinsulinemia, hypertrophy and hyperplasia of adipocytes, and impaired fertility. In contrast with other diabetic strains of mice, glycemia was normal in females and slightly elevated in males. This result indicates that the mutation of the db locus does not necessarily lead to a frank diabetes. Body temperature was normal either at 22 degrees C or after a cold exposure at 4 degrees C. GDP (guanosine diphosphate) binding to brown adipose tissue mitochondria was normal in obese mice as compared to lean. These data differentiate this model from other genetic obesities in mice and rats. This new model of genetic obesity offers interesting characteristics for the study of obesity.
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PMID:Description of a new model of genetic obesity: the dbPas mouse. 388 10

Cold-exposed rats exhibit hypermetabolism, hyperphagia, and increased glucose oxidation. Their counterregulatory hormone secretion is markedly elevated, while insulin levels fall acutely, gradually returning to basal during acclimation. We assessed both hepatic and peripheral sensitivity to insulin in rats in the basal state and after 5 days of cold (5 C) exposure. The contribution of gluconeogenesis to total glucose turnover was measured and compared to daily urinary corticosterone excretion. Hepatic glucose production was equally suppressed by the infusion of insulin at 1.2 mU/kg X min in both control and cold-acclimated rats, but enhanced hepatic sensitivity to low dose (0.6 mU/kg X min) insulin infusion was only observed after cold exposure. The metabolic clearance of glucose was elevated with cold stress and was insensitive to the infusion of insulin at either level. Insulin resistance was not observed. Urinary excretion of corticosterone and urea nitrogen were markedly increased, but creatinine excretion was unchanged, suggesting that the concurrent increase in gluconeogenesis resulted from increased protein intake rather than increased catabolism of muscle protein.
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PMID:Enhanced hepatic insulin sensitivity and peripheral glucose uptake in cold acclimating rats. 389 63


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